The Presidential Coronary Calcium Score and the Power of Zero

 

“Maybe I’ll win

Saved by zero”

The Fixx, 1983

 

Since the 1990’s, the U.S. Presidents and the Presidential candidates have undergone coronary calcium scores. What can we learn from their results? Let’s look at two examples. Let’s call them the Clintons. Hillary Clinton reportedly had a coronary calcium score of 0. As far as we know, she has not had any heart disease. Bill Clinton’s coronary calcium score was over 1000. He subsequently required open heart bypass surgery. Can you guess the coronary calcium scores of Presidents George Bush, Barack Obama and Donald Trump? What is the coronary calcium score and can you be “saved by zero”?

 

To understand coronary calcium, we must understand the process of atherosclerosis in the heart arteries. In susceptible individuals, plaque formation starts at an early age, the 20’s and 30’s. The initial plaque in the heart arteries is made of cholesterol, what is called “soft” plaque or “fatty” plaque. If we did a CT scan at this stage, no calcium would be detected. Over time, plaque progression continues and by the age of 50 to 60, calcium is deposited in the plaque. The plaque is now considered “hard” plaque. At this stage, a CT scan would detect calcium in the artery. Coronary calcium therefore detects the presence of plaque in the heart arteries. It does not tell us if the plaque is limited to the artery wall or if the plaque is causing significant blockage to the blood flow (obstruction can be determined with a stress test or a heart catheterization).  

 

What is the coronary calcium score and how is it used? Coronary calcium score is obtained with a CT scan. There is no fasting, no preparation, no intravenous and no dye used. The person goes under the CT scanner, holds their breath for about one minute, the scan is taken and done. What do the results mean? For people between the ages of 40 and 75 without established heart artery disease, the score is used as follows. A score greater than 100 represents extensive plaque and an increased risk for future cardiac events (heart attack, blocked heart artery, stroke, cardiac death). In this case a statin (and perhaps aspirin 81 mg once per day) is recommended. A score between 1 and 99 is intermediate. Even a low calcium score (between 1 and 10) is associated with a two times greater risk for cardiac events compared to score of zero. In this population, a statin is recommended if high risk characteristics are present (age over 55, family history of premature heart disease, persistently elevated LDL cholesterol or triglycerides, evidence for inflammation or elevated lipoprotein a in the blood). 

 

What does a coronary calcium score of zero represent? There are two clinical possibilities. One is that there is no heart artery plaque. The other scenario is that there is soft or fatty plaque present, which has not yet calcified. Most studies have found that among patients with coronary calcium of zero, there is a very low likelihood of blockage in the heart arteries and a low risk for heart events (heart attack, stroke, death). However, one study looked at 10,000 people and found that 45% of them had a coronary score of zero. Among those with zero scores, 1.8% still had at least one artery blocked 50% or greater. The prognostic value of a zero score was less for those under the age of 45 (they likely had not had enough time for the plaque to calcify). In general, a coronary calcium score of zero is a good prognostic sign. How long does that prognostic value last? What is the warranty period of a calcium score of zero? A study showed that about 15% of people with initial calcium score of zero progressed to a score over 10 in about 5 to 8 years. In the study it was rare to progress to a calcium score over 100. Diabetic patients, active smokers and those with strong family history progressed more quickly. Based on these data, it is recommended that statin therapy be withheld for a patient with a calcium score of zero, unless they have diabetes, are smoking or there is a family history of premature heart disease. How often should the calcium score be repeated to reassess risk? For patients with a coronary calcium score of zero, repeating the study is recommended in 3 to 5 years. For patients with an elevated coronary calcium score who are already on statin, it is not recommended to have a follow up study. The reason is that the calcium score may go up on statin treatment. If the score goes up, we don’t know if there has been further plaque progression or increasing calcium in existing plaque- a sign of healing.

 

Using the coronary calcium can help predict the risk for future heart events in patients between 40 and 75 years old who have not yet had a cardiac issue (primary prevention). If you are like Bill and your coronary calcium score is greater than zero, initiating lifestyle changes and starting a statin can reduce the risk for a heart event in the future. If you are lucky like Hillary and your coronary calcium score is zero, the risk for future events is low. However, it is not a “get out jail free” card nor are you “saved by zero”. If coronary calcium score is zero and LDL cholesterol is high, then lifestyle changes should be incorporated even if starting a statin may be avoided. Vigilance is necessary with follow up lipid panels and repeat coronary calcium testing in 3 to 5 years. 

POTS or Why Am I Dizzy When I Stand Up?

 

When you think about, we shouldn’t be able to stand upright. Our ancient ancestors, floating around in the sea, used the water for everything; hydration, nutrition and support. The water buoyed them, there was no need for a spine or other elaborate bony structures. To leave the water and especially to walk upright on two legs, certain adaptations were needed. Skeletal features that evolved over time included a spine, hip bones, thigh bones and the muscles needed to keep the body upright and erect. Circulatory adaptations were needed as well. When we are upright, the heart has to pump blood against gravity to keep blood flowing to the brain. Blood pressure to the brain must be maintained otherwise when we stand up, the blood pressure would drop, the blood flow to the brain would decrease and we would pass out. How does the circulation respond to standing and why don’t we routinely pass out?

 

The mechanism that evolved to keep us upright is a blood pressure feedback loop that involves the heart, the brain and the blood vessels. On standing, blood pools in the veins in the legs. This causes a transient decrease in blood pressure. This drop in blood pressure is recognized by a sensor in the carotid artery (the carotid artery is the main artery supplying blood to the brain, the sensor is located in the carotid sinus, just outside of the skull). When the carotid sinus senses a lower blood pressure, it fires nerves which activate the sympathetic system. The sympathetic system constricts blood vessels, increases the heart rate and increases the amount of blood pumped by the heart ultimately restoring normal blood pressure to the brain and preventing passing out.

 

This mechanism is very effective at maintaining blood pressure. However, there are circumstances where the mechanism is overwhelmed causing dizziness or passing out. Instances include prolonged standing in a hot environment (think of a soldier standing for a long time in the hot sun), dehydration, or deconditioning from staying in bed for a long time. As we age, the mechanism isn’t as fast and we can have dizziness on rising quickly from a sitting or lying down position. If the mechanism isn’t working, it leads to passing out on standing, a condition called orthostatic hypotension (from the Greek ortho- straight and statikos- causing to stand; caused by standing erect; hypotension- low blood pressure). Orthostatic hypotension is defined as a drop in systolic blood pressure of 20 mmHg or more within three minutes of standing. It is a significant medical problem whose incidence rises after age 65. It occurs in 6% of elderly people in the community and up to 50% of people in nursing homes. Orthostatic hypotension puts patients at risk for falls, as well as cardiac disease. Orthostatic hypotension occurs in patients with degenerative diseases of the autonomic nervous system (for example, Parkinson’s disease). It also occurs due to an impaired autonomic nervous system (for example, diabetes). Orthostatic hypotension can be diagnosed in the office or at the hospital bedside by checking blood pressure lying down and standing up. The formal way to diagnose it is with a tilt table test (strapping a patient to an upright table and checking blood pressure frequently). 

 

There are multiple ways to treat orthostatic hypotension. In milder forms, patients recognize that they are about to pass out and can sit or lay down to avoid falling. For more significant cases, the first step is to stop medications that can lower the blood pressure or exaggerate orthostatic symptoms. Medications to avoid include diuretics, most blood pressure meds, prostate medications (ex, Flomax or tamsulosin), antiparkinson agents and antidepressants. Other measures include increasing blood volume by keeping hydrated, ingesting salt tablets, or using a medication (fludrocortisone) which promotes salt retention. Pooling of blood in the veins of the lower legs can be decreased by using compression stockings. Lastly, medications that stimulate the sympathetic nervous system (such as midodrine or droxidopa, Northera) can be used. 

 

POTS (postural orthostatic tachycardia syndrome) is the most common form of orthostatic intolerance in young people. It usual affects young, pre-menopausal women with as many as 500,000 cases in the US. It is defined as an increase in the heart rate of 30 beats per minute or more within 10 minutes of standing, but without a decrease in blood pressure. The typical patient is a 30-year-old woman with a heart rate increment of 40 beats per min or more. Cardiovascular deconditioning is common. Therefore, the key to treatment is exercise. The exercise regimen should avoid the upright position (swimming or recumbent bike can be prescribed) until fitness improves. Liberal intake of fluids and salt, compression stockings and sleeping with the head of the bed greater than 30 degrees are other methods. Medications can be used in severe cases and include the same agents used for orthostatic hypotension. 

 

Whether you are young or old, if you have dizziness on rising there are measures you can take to avoid symptoms. If you have more severe symptoms or are passing out on standing, see your doctor to work through how to keep yourself upright. 

How Sweet It Is!

 

Ralph: (growling) Where's my morning coffee?

Alice: Here you go Ralph

Ralph: (sipping) That tastes terrible!

Alice: We ran out of sugar

Ralph: One of these days, Alice. One of these days. 

Alice: Try this new artificial sweetener

Ralph (sipping) How sweet it is!

 

If you are of a certain age, you can identify these characters from the 1950’s television show "The Honeymooners" and you’ll recognize the Ralph Kramden/Jackie Gleason catchphrase, "How sweet it is!". So how sweet are artificial sweeteners? Depending on the agent, artificial sweeteners are 200 to 600 times sweeter than sugar. However, are they healthier than sugar? Are there any heart issues with artificial sweeteners?

 

Sugar seems to be the new bad guy on the block, not without reason. Everyone likes a sugary snack every now and then, but can it be limited to just one snack? Sugar triggers a reaction in our brain and makes us crave more. Sugar begets sugar. So, instead of stopping at one serving, more sugar is desired and before you know it, the whole candy bar is gone. All that sugar consumption adds empty calories, resulting in obesity, diabetes and heart disease. Even natural sweeteners, such as honey or molasses are a form of added sugar and add calories to the diet. To counteract the health effects of sugar, artificial sweeteners were developed and have been available for decades. Artificial sweeteners taste sweet like sugar but have no or few calories. They allow people to enjoy the sweetness of foods and drinks but without excess calories.  In this way, artificial sweeteners can help with weight loss. US and European health agencies have deemed artificial sweeteners safe in limited amounts and extensive research has not shown a higher risk of cancer. It had been felt that these sugar substitutes do not cause serious health problems. Until now.

 

Recent research on artificially sweetened beverages has shown a link to heart disease. A French study started in 2009 and including 104,000 participants found that people who drank 6 ounces or more per day of artificially sweetened beverages had a higher risk for cardiovascular disease. Artificial sweetened beverages included drinks that contained aspartame (also used in NutraSweet, Equal) and sucralose (found in Splenda). Another study of 9000 participants followed for 10 years showed that those who drank greater than two liters per week (about 10 ounces per day) of an artificially sweetened beverage had an increased risk for atrial fibrillation. One last study followed 2,888 participants and found artificially sweetened drinks to be associated with a higher risk of stroke and dementia. So, these beverages may not be a healthy substitute for sugary soft drinks.

 

The data on two artificial sweeteners, both from the sugar alcohol category, seems especially troubling. Erythritol is a no calorie sugar substitute used in many products including protein bars, yogurt, cookies and ice cream. It occurs naturally in melons and grapes. It is also the primary sweetener in the low carbohydrate high fat keto diet. A 2023 study of 1100 people found that high levels of erythritol in the blood was associated with an increased risk of heart attack, stroke and death. A more recent study may explain why. Twenty healthy volunteers were given drinks sweetened with a typical amount of erythritol or a drink with sugar. When given erythritol, the blood platelets were activated putting people at risk for blood clotting, heart attack or stroke. The same platelet effect was not seen when consuming a sugar drink. Another sugar alcohol artificial sweetener, xylitol, has similar data. Xylitol is found naturally in fruit and vegetables. It is also used to sweeten gum and toothpaste. In a study of 3000 people in the US and Europe, those with the highest level of xylitol in the blood were more likely to have heart or blood vessel problems. Another study followed 1100 people for three years. Xylitol was associated with major adverse cardiac events and was shown to activate platelets, similar to erythritol. 

 

As daunting as this data is, experts have not declared any artificial sweetener a cardiac risk. However, more and better research is needed on these agents, especially the potential cardiovascular effects. Before you declare “How sweet it is!” and consume artificial sweeteners with impunity, keep an eye out for future research on the safety of these agents. For now, using them in small, limited quantities seems to be safe. 

 

The Siesta

The Siesta (or La Meridienne in French) is a famous painting by the artist Vincent Van Gogh. It depicts a siesta and symbolizes life in rural France in the late 1880’s. Siesta is a Spanish word meaning a short nap, usually taken in the afternoon, after lunch. In warm weather climates workers who do physical labor need to take a break to avoid the hottest part of the day. Siestas are common in Mediterranean countries, the Middle East, China, Latin America and the Philippines. Siestas are both practical and cultural. There are studies from Greece showing that naps are associated with a lower risk for heart attack. What is the data on siestas? How does day time napping affect cardiac health?

 

The health data on siestas is quite variable, showing some good and some bad effects. In a study from 2019, taking a daytime nap was associated with lower blood pressure. In those that nap, the blood pressure was 5 mmHg lower than in those that didn’t nap. Usually when something lowers blood pressure there is concomitant lowering of cardiac risk.  That doesn’t seem to be the case with napping. A comprehensive review of relevant studies showed that daytime napping over 60 minutes was associated with an increased risk for cardiac disease and mortality.  Another study followed 116, 000 people for 8 years and found that napping was associated with increased for major cardiac events and death in those that slept on average more than six hours per night. No increased risk was found in people who slept less than 6 hours per night. It was felt that naps compensated for lack of sleep for people who didn’t get enough sleep at night. The most recent study found some disturbing trends. The trial studied 476,000 people determining that 56% never or rarely took a nap, 38% sometimes napped and 5% usually took a daytime nap. Compared to people who never or rarely napped, frequent daytime napping increased the risk for atrial fibrillation and for dementia. This is the first time this association was made regarding the siesta. Why does napping lead to atrial fibrillation? One hypothesis is that napping indicates inadequate nighttime sleep from undiagnosed sleep apnea, a condition well known to cause atrial fibrillation. In addition, atrial fibrillation is a risk for dementia. 

 

It appears that frequent daytime napping can lead to dementia. What is the optimal amount of sleep to avoid dementia? The largest sleep study ever conducted just finished and concluded that 7 hours of sleep per night was the right amount for reasoning, verbal skills and overall cognitive thinking.  Sleeping more or less than that could lead to cognitive decline and dementia. What other new data has emerged regarding dementia? Eating processed red meat and sugar have been associated with dementia. Processed red meat (including bacon, hot dogs, sausages, salami, cold cuts) has been tied to an increased risk of cancer, heart disease and diabetes. A new study that tracked 100,000 people over four decades showed that eating two servings of red meat each week increased the risk for dementia by 14% and was associated with worse memory and thinking skills. The study also showed that replacing red meat with nuts, beans or tofu lowered the risk for cognitive decline by 23%. Processed red meat may affect the brain because of harmful chemicals such as nitrites and the increased sodium content can lead to high blood pressure. The study only found an association but did not prove cause and effect. So, we don’t know if red meat itself causes dementia or if people who avoid red meat are generally more health conscious. Unprocessed red meat, such as ground beef or steak, was not linked to dementia in the trial. In other news, on World Brain Day (July 22 2024), the German Society of Neurology warned that too much sugar can harm the brain.  High blood sugar levels can damage blood vessels, causing plaque, decreasing blood flow and causing vascular dementia. In addition, sugar directly affects the nerve cells, impairing cognition. What should be eaten instead? Try to eat whole fresh foods (fruits, vegetables, fish, nuts, beans) and the less processed, the better. Whole fresh foods bring protein, fiber, nutrients, minerals and vitamins the brain promoting a healthier body and longer lifespan.

 

Last month we found out that to decrease your risk for dementia you should take your blood pressure medications, go to the shore, plop down on a beach chair and watch the waves roll in. This month we learn that, to further lower your risk for dementia, try not to nap in that beach chair. In addition, skip the hot dog, ice cream and cotton candy on the boardwalk. It is hard to do, but it may be well worth it. 

Beach Blanket Blood Pressure

 

It’s July! Summer time! Time to vacation and unwind. Head to your favorite beach, plop down on your beach chair and watch the waves role in. You can feel yourself relaxing, calming down. You can actually feel your blood pressure (BP) dropping. Does the presence of water really lower BP? Researchers actually did this study. They found that viewing water in an outdoor setting (for example a lake) reliably lowered BP compared to looking at grass field. Aside from water watching, what else is new in the world of hypertension (high blood pressure)?

 

Before diving into new data, some basics about hypertension. Despite knowing about high BP for more than 100 years and despite the fact that nearly 50% of the population has hypertension, we still do not know what causes it. What is the definition of hypertension? Hypertension is diagnosed as a BP greater than 130/80 on multiple occasions over several weeks. What is the ideal BP? 115/75. Several studies have shown that treating BP to under 120 mmHg improved outcomes versus treating to a BP under 140 mmHg. The under 120 mmHg group had fewer heart events, lower mortality and less cognitive decline. It is important to understand that the BP is not one single, stable number. Rather BP goes up and down, like waves on the ocean, with activity, time of day, and medications among other factors. The goal is to have nice, calm undulating waves of BP, not tidal waves with extreme highs and very low lows. Also, the goal is to have the BP average under 140 mmHg, or more ideally, under 120 mmHg. Hypertension is treated with lifestyle modifications and medications. Lifestyle changes include exercise, weight loss, smoking cessation and following a DASH diet. Sodium reduction (a low salt diet) is also important for treatment. First line medications for hypertension fall into three classes of drugs: diuretics (hydrocholorothiazide, chlorthalidone), calcium channel blockers (amlodipine) and angiotension converting enzyme inhibitors (lisinopril, ramipril) or angiotension receptor blockers (losartan, olmesartan). Reducing BP with medications reduces the risk of dying, reduces stroke by 35-40%, reduces heart attack by 20-25%, reduces heart failure by more than 50% and decreases the risk for dementia and cognitive impairment. 

 

Of the three classes of medications, which one is best? A recent study followed 33,000 patients for 23 years looking at the three types of medications and assessing outcomes. The researchers found no difference among the three classes in their BP lowering efficacy and no difference in cardiovascular mortality or stroke. 

 

In this era of BP medications is a low salt diet still recommended? High sodium (salt) intake has long been associated with hypertension. BP clearly goes up with sodium intake of 2 grams per day (2 grams of sodium is about 88% of a teaspoon of table salt). It is estimated that Americans eat on average 3.4 grams of salt per day. The optimal goal for salt intake is about 1.5 grams per day. Lowering sodium intake can reduce BP by 5 to 6 mmHg. Does this effect persist if patients are already on BP meds? A recent trial studied 213 people on BP medications. They were given a high sodium diet for one week, then a low sodium diet the second week and their BPs were tracked. BP was 8 mmHg higher on the high sodium diet. The low sodium diet consistently lowered BP, on top of the presence of medication. The conclusion, “Don’t underestimate the power of salt”.

 

Elevated systolic BP is linked to mild cognitive impairment and dementia. Hypertension may cause dementia by direct and indirect methods. A direct mechanism is the known risk between hypertension and stroke. Multiple small strokes due to elevated BP can cause dementia over time. An indirect mechanism is atrial fibrillation. Hypertension is associated with atrial fibrillation, which in turn can cause blood clots which break off from the heart and travel to the brain. It has long been felt, but not proven, that BP lowering reduced the risk for dementia. However, new data is beginning to emerge. Now we have learned that just by taking medication, dementia can be avoided. A study from Italy followed 215,000 patients for seven years. The patients were starting BP medications for the first time. It was found that the patients who were more adherent to their BP meds (more likely to take their meds) had lower odds of going on to dementia. Another recent study was the first definitive trial to show that BP reduction lowered the risk for dementia. The study looked at 34,000 patients age 40 and older. In patients with intensive BP reduction (goal < 130/80), dementia was lowered by 15% and cognitive impairment improved as well. These results are exciting because now there is a potential tool to prevent dementia. 

 

In order to control your blood pressure and reduce your risk for dementia this summer, don’t forget to take your medications regularly, follow a low salt diet and head out to the beach.

 

 

 

Fun With Stress (How to Read the Exercise Stress Test Report)

 

If you are having heart symptoms (chest pain or shortness of breath, especially with exertion), your doctor may order an exercise stress test to see if the symptoms are related to underlying heart disease. Approximately 10 million exercise stress tests are done in the US each year. What is an exercise stress test? What is it used for? What information does it provide and how can that information be used?

 

With the exercise stress test, the patient is attached to an EKG machine and a blood pressure cuff is placed on the arm.  The patient then walks on the treadmill according to protocol. The most commonly used protocol is the Bruce protocol, developed by Dr Robert Bruce and in use since around 1963. The Bruce protocol starts at 1.7 mph and a 10% incline. Every three minutes, the treadmill goes higher and faster. Stage 2 of the Bruce protocol is 2.5 mph with a 12% incline, Stage 3 is 3.4 mph, 14%, and so on. During the stress test, the patient is monitored for symptoms (chest pain, shortness of breath), the blood pressure is checked every stage and an EKG is done at the end of each stage. The test is terminated if the patient has chest pain, can’t exercise further, develops changes on the EKG (ST segment depression), develops a significant arrhythmia or the blood pressure goes too high. 

 

Let’s look at a typical report (shown above). Under “Exercise Test Summary” is the raw data; stage, time in stage, treadmill speed (mph), grade (%), heart rate (HR) and blood pressure (BP). This patient exercised for 7 minutes 23 seconds of a Bruce protocol, 3 minutes each in stages 1 and 2 and 1 minute 23 seconds in stage 3. The person achieved a work load of 10.4 METs. The metabolic equivalent of task (MET) is an estimation of the person’s exercise capacity, based on how many minutes of the Bruce protocol is achieved. The resting heart rate was 81 BPM and rose to 166 BPM or 92% of the predicated maximal heart rate. The heart rate should increase as the work load increases (work load increases with each progressive stage). Before the test, each person’s maximal heart rate is calculated. During the test, exercise continues until the patient achieves at least 85% of their predicated maximal heart rate. A rough estimate of the maximal heart rate is:

            Max HR = 220 – age

More precise estimates are used based on age and sex:

            Men:                Max HR = 208- (0.7 x age)

            Women:          Max HR= 206 – (0.88 x age)

The blood pressure was 128/80 mmHg at rest and 166/80 mmHg at peak exercise. The systolic blood pressure increases linearly with each stage and returns to baseline or, more often, below the baseline in the recovery period. The average increase in systolic blood pressure with exercise is about 30 to 40 mmHg. A blood pressure over 200 to 210 mmHg represents exercise induced hypertension. Diastolic blood pressure usually stays about the same during exercise. This test was terminated due to fatigue and the person had no chest pain. There were occasional PVCs (premature ventricular contractions, extra beats from the lower chamber of the heart). There were some ST segment changes, 0.5-1.0 mm horizontal ST segment depression. ST segment changes of more than 1.0 mm are considered abnormal.  Horizontal ST segment depression is worse than upsloping depression. Downsloping ST segment depression is worse than horizontal. The test was interpreted as normal. 

 

The main indication for an exercise stress test is to see if there is myocardial ischemia (lack of blood flow to the heart muscle due to blockage in a heart artery). Ischemia is present if the patient has chest pain or if there are diagnostic ST segment changes. However, the stress test is not ideal. The diagnostic accuracy for heart artery blockage is only about 70%, so it misses about 30% of the time. Other tests, such as a nuclear stress test (accuracy 85-90%), CT imaging of the heart arteries or cardiac catheterization are more accurate in picking out significant heart artery disease. Despite this, there is a lot of useful information to be gleaned from the exercise stress test. Exercise or functional capacity is a strong predictor of mortality and heart disease. The better the exercise capacity, the lower the risk of cardiac outcomes. Functional capacity is measured in METs. As we saw, METs are calculated and shown on the stress test report. To determine if the number of METs achieved is good, here are the formulas for average METs for men and women:

            Men:                Predicted METs= 18 – (0.15 x age)

            Women:          Predicted METs= 14.7- (0.13 x age) 

If the METs on your stress test are higher than the predicted, your functional capacity is good or high. If lower, then functional capacity is fair or poor. The data from an exercise stress test may also be used to formulate a personalized exercise prescription. For more information about exercise prescription see: http://sportscardiology.blogspot.com/2017/08/an-exercise-prescription-to-get-fitt.html

 

The exercise stress test can also predict prognosis. In general, the longer on the treadmill and the better the exercise capacity, the lower the risk for heart outcomes. Functional capacity is the most important parameter. Other prognostic variables include heart rate achieved, heart rate and blood pressure response to exercise, exercise induced chest pain and ST segment changes. To quantify prognosis, the Duke Treadmill Score was developed and has been in use since the early 1990’s. The score uses three variables: 1- exercise time, 2- ST segment changes, 3- presence or absence of chest pain. The formula is:

            Duke Treadmill Score= exercise time – (5 x ST segment deviation) – (4 x CP index)

ST segment deviation is 0.5 mm, 1.0 mm, 1.5 mm, 2.0 mm, 2.5 mm, etc. CP index is 0 if there is no chest pain during exercise, 1 if there is chest pain, but the patient can still exercise through it, 3- if chest pain causes the test to be stopped. The Duke Treadmill Score ranges from -25 (highest risk) to + 15 (lowest risk). The one-year mortality for the low-risk category (score >=5) is only 0.25% but in the high-risk category (<= - 11) the mortality at one year is 5.25%. 

 

In addition to all of the above, the exercise stress test is used to determine the heart rate response to exercise (whether the heart rate increases appropriately), the blood pressure response (whether the blood pressure goes up too high or drops during exercise, either scenario being a high-risk characteristic) and to see if there are exercise induced rhythm problems.        

 

Aside from diagnosing heart artery disease, the exercise stress test provides a wealth of information that is important both for the physician and patient. Armed with the formulas above and a copy of your stress test report, you can have lots of fun. You can calculate your maximum heart rate (then take 85% of that to determine your target heart rate during exercise). You can determine your functional capacity (METs) and see how you stack up against the general public. You can calculate your Duke Treadmill Score. So sharpen your pencil, get your calculator out and get to work.

 

 

How To Read The Lipid Panel

You try to be a good patient. You schedule your general physical with your primary doctor every year. Your doctor sends you for blood work, which you have done. Once the results are available, you log into your patient portal. There they are, your lab results. However, you are confused. What do all those initials mean? What do the numbers mean? Which ones are relevant? Which ones should you ignore? Here is a general primer on how to read your lipid panel blood test.

Before we look at some test results, we need some definitions. Lipids are a broad group of molecules that include cholesterol, triglycerides, fatty acids and others. Lipids are involved in many biologic functions. Lipids don’t dissolve in the blood and have to be transported from where they enter the body (or are stored) to the site where needed. Apolipoproteins carry out the transportation of lipids. 

Now, let’s walk through some typical lipid panel results. We’ll start with the panel pictured above. The first line is Total Cholesterol, which in this case is 121 mg/dl. In general, cholesterol levels should be below 200 mg/dl. Total cholesterol is a marginally useful number. The next line shows the triglycerides, which are 46 mg/dl. Triglycerides are the fat in the blood. When we eat food, any excess calories are turned into triglycerides and stored in fat cells. When extra energy is required by the body, the triglycerides are released and used. Triglycerides and cholesterol are different types of lipids. Triglycerides are used for energy while cholesterol is used to build cells and proteins. A normal triglyceride level is less than 150 mg/dl. An elevated triglyceride level (over 150 mg/dl) is associated with excess risk for heart artery disease, heart attack and cardiac death. The next line is HDL Cholesterol at 67 mg/dl. HDL stands for High Density Lipoprotein. It is the “good” cholesterol. HDL transports excess cholesterol in the body back to the liver where it is metabolized and excreted. HDL is important. Low levels of HDL have consistently been associated with heart artery disease. However, the converse is not true; high levels of HDL do not protect against heart artery blockage, contrary to the urban myth that it does. Many patients when asked why they are not on medication for their high cholesterol state that it is because they have a high HDL. HDL levels above 39 mg/dl are ideal. Many studies involving many different medications have been tried to raise HDL. Unfortunately, no pharmacologic therapy has been proven to raise HDL and reduce cardiac outcomes. The next line is VLDL Cholesterol Cal at 11 mg/dl. VLDL stands for Very Low Density Lipoprotein and these particles travel with triglycerides. The VLDL value is not measured but calculated (thus the ”Cal”) as trigylcerides divided by 5. It is not a clinically useful value and can be ignored. 

The next line is the most important, LDL Chol Calc (NIH) at 43 mg/dl. LDL is Low Density Lipoprotein and this can be reported in two different ways. It can be measured directly, which not the usual case as it is difficult. Most of the time, it is a calculated value. There are at least three different formulas for calculating LDL. The simplest is the Friedewald equation where LDL= total cholesterol- (HDL+triglycerides/5). Other equations are the NIH (which is the one used in the example) and Martin-Hopkins formula. There are differences in the equations, but a recent study found that the differences are small and not clinically significant. Excess LDL builds up in the artery wall, forming plaque and leading to blockage which results in a heart attack or stroke. As the average LDL level rises, the chance of atherosclerosis/plaque goes up and the number of sites affected goes up as well. In general, the LDL should be less than 100 mg/dl. In patients who have had a heart attack or stroke or had a stent or heart bypass, the LDL goal is less than 70 mg/dl or even lower. The last line is the LDL/HDL ratio. This number is irrelevant and can be ignored; just concentrate on the actual numbers, especially LDL, HDL and triglycerides.

Here is another example of a lipid panel report. It has two new parameters, Cholesterol/HDL ratio and non HDL cholesterol. As with the LDL/HDL ratio the cholesterol/HDL ratio has no clinical relevance and can be ignored. The non HDL cholesterol is important. Non HDL cholesterol is a measure of the all of the atherogenic lipids molecules. It is a best estimate of all of the important lipids that cause plaque and blockage. The formula for non HDL cholesterol is simple: Total cholesterol – HDL. The ideal value for non HDL cholesterol is less than 130 mg/dl. 

So, this is how to interpret the basic lipid panel. What about advanced tests? What is available? What is useful? There is a test called the NMR Lipoprofile. It reports more in-depth parameters such as particle size and density. While there is some slight incremental value in these numbers in terms of cardiac risk evaluation, no cardiac society recommends it. The consensus is that the standard lipid panel is good enough to estimate and follow risk. One test that may be beneficial is Apo B. Remember that apolipoproteins transport cholesterol in the blood. Apo B is one of those transport proteins and it carries all of the atherogenic lipids: LDL, VLDL and Lipoprotein a (more about this in a bit). So, measuring Apo B gives a very good sense of how much risk of atherosclerosis is present. Apo B is a more accurate marker of cardiac risk than LDL or non HDL cholesterol. The difference may or may not be clinically relevant. Currently, Apo B is not routinely checked but that may change in the future. Lipoprotein a is a lipid particle that is 5 times more atherogenic than LDL. It runs in families and it is estimated that one in five people have an elevated lipoprotein a level. A lipoprotein a level should be checked if there is a strong family history for premature heart artery disease or if a patient has recurrent heart attacks despite low levels of LDL. Lipoprotein a levels less than 75 mg/dl are considered normal.

In summary, the basic lipid panel provides enough information for risk assessment and for following progress in the prevention of coronary artery disease. The important numbers to pay attention to, in order, are: LDL, HDL, Triglycerides, non HDL cholesterol and finally total cholesterol.

 

Additional resources:

LDL:

http://sportscardiology.blogspot.com/2022/03/cholesterol-years.html

 

HDL:

http://sportscardiology.blogspot.com/2022/10/how-high-is-too-high.html

 

Triglycerides:

http://sportscardiology.blogspot.com/2023/11/the-trouble-with-triglycerides.html

 

Lipoprotein a:

http://sportscardiology.blogspot.com/2021/04/